A pathologic condition of acid accumulation or depletion of base in the body. The two main types are RESPIRATORY ACIDOSIS and metabolic acidosis, due to metabolic acid build up.
Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized. It may occur spontaneously or in association with diseases such as DIABETES MELLITUS; LEUKEMIA; or LIVER FAILURE.
Respiratory retention of carbon dioxide. It may be chronic or acute.
A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS.
The balance between acids and bases in the BODY FLUIDS. The pH (HYDROGEN-ION CONCENTRATION) of the arterial BLOOD provides an index for the total body acid-base balance.
Inorganic salts that contain the -HCO3 radical. They are an important factor in determining the pH of the blood and the concentration of bicarbonate ions is regulated by the kidney. Levels in the blood are an index of the alkali reserve or buffering capacity.
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.
A pathological condition that removes acid or adds base to the body fluids.
An acidifying agent that has expectorant and diuretic effects. Also used in etching and batteries and as a flux in electroplating.
A mitochondrial disorder characterized by focal or generalized seizures, episodes of transient or persistent neurologic dysfunction resembling strokes, and ragged-red fibers on muscle biopsy. Affected individuals tend to be normal at birth through early childhood, then experience growth failure, episodic vomiting, and recurrent cerebral insults resulting in visual loss and hemiparesis. The cortical lesions tend to occur in the parietal and occipital lobes and are not associated with vascular occlusion. VASCULAR HEADACHE is frequently associated and the disorder tends to be familial. (From Joynt, Clinical Neurology, 1992, Ch56, p117)
A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals.
Disturbances in the ACID-BASE EQUILIBRIUM of the body.
A life-threatening complication of diabetes mellitus, primarily of TYPE 1 DIABETES MELLITUS with severe INSULIN deficiency and extreme HYPERGLYCEMIA. It is characterized by KETOSIS; DEHYDRATION; and depressed consciousness leading to COMA.
Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.
A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood.
A state due to excess loss of carbon dioxide from the body. (Dorland, 27th ed)
A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)
Measurement of oxygen and carbon dioxide in the blood.
A powder that dissolves in water, which is administered orally, and is used as a diuretic, expectorant, systemic alkalizer, and electrolyte replenisher.
A biguanide hypoglycemic agent with actions and uses similar to those of METFORMIN. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290)
A plasma membrane exchange glycoprotein transporter that functions in intracellular pH regulation, cell volume regulation, and cellular response to many different hormones and mitogens.
A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. Note that the aqueous form of ammonia is referred to as AMMONIUM HYDROXIDE.
Proteins that cotransport sodium ions and bicarbonate ions across cellular membranes.
Chemical compounds which yield hydrogen ions or protons when dissolved in water, whose hydrogen can be replaced by metals or basic radicals, or which react with bases to form salts and water (neutralization). An extension of the term includes substances dissolved in media other than water. (Grant & Hackh's Chemical Dictionary, 5th ed)
A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. GASTRIC ACID is the hydrochloric acid component of GASTRIC JUICE.
Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)
Abnormally high potassium concentration in the blood, most often due to defective renal excretion. It is characterized clinically by electrocardiographic abnormalities (elevated T waves and depressed P waves, and eventually by atrial asystole). In severe cases, weakness and flaccid paralysis may occur. (Dorland, 27th ed)
A hereditary or acquired form of generalized dysfunction of the PROXIMAL KIDNEY TUBULE without primary involvement of the KIDNEY GLOMERULUS. It is usually characterized by the tubular wasting of nutrients and salts (GLUCOSE; AMINO ACIDS; PHOSPHATES; and BICARBONATES) resulting in HYPOKALEMIA; ACIDOSIS; HYPERCALCIURIA; and PROTEINURIA.
A transfer RNA which is specific for carrying leucine to sites on the ribosomes in preparation for protein synthesis.
A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.
The pressure that would be exerted by one component of a mixture of gases if it were present alone in a container. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Glutaminase is an enzyme that catalyzes the conversion of glutamine to glutamate and ammonia, playing a crucial role in nitrogen metabolism and amino acid homeostasis within various tissues and cells, including the brain, kidney, and immune cells.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
A derivative of ACETIC ACID that contains two CHLORINE atoms attached to its methyl group.
A condition characterized by calcification of the renal tissue itself. It is usually seen in distal RENAL TUBULAR ACIDOSIS with calcium deposition in the DISTAL KIDNEY TUBULES and the surrounding interstitium. Nephrocalcinosis causes RENAL INSUFFICIENCY.
The first stomach of ruminants. It lies on the left side of the body, occupying the whole of the left side of the abdomen and even stretching across the median plane of the body to the right side. It is capacious, divided into an upper and a lower sac, each of which has a blind sac at its posterior extremity. The rumen is lined by mucous membrane containing no digestive glands, but mucus-secreting glands are present in large numbers. Coarse, partially chewed food is stored and churned in the rumen until the animal finds circumstances convenient for rumination. When this occurs, little balls of food are regurgitated through the esophagus into the mouth, and are subjected to a second more thorough mastication, swallowed, and passed on into other parts of the compound stomach. (From Black's Veterinary Dictionary, 17th ed)

Hypokalaemic paralysis revealing Sjogren syndrome in an elderly man. (1/246)

A 73 year old white man presented with life threatening hypokalaemic paralysis requiring admission to an intensive care unit. Biochemical investigations showed severe hypokalaemia with hyperchloraemic metabolic acidosis, a spot urine pH of 6.5, and a positive urinary anion gap, establishing the diagnosis of distal renal tubular acidosis. Autoimmune tests revealed Sjogren syndrome as the underlying cause of the distal renal tubular acidosis. Full recovery followed potassium and alkali replacement. This dramatic presentation of Sjogren syndrome has not previously been reported in an elderly man.  (+info)

The occurrence of renal involvement in primary Sjogren's syndrome: a study of 78 patients. (2/246)

OBJECTIVE: To ascertain the occurrence of renal involvement in patients with primary Sjogren's syndrome (pSS). METHODS: Urinary total protein excretion from 24 h urine collection, as well as urinary excretion rates of albumin, alpha-1 microglobulin (alpha1m) and IgG from overnight 8 h collections, were determined from 78 pSS patients (75 females, three males). Urine acidification capacity after oral ammonium chloride load was tested in 55 of these patients. RESULTS: Mild proteinuria (0.15-0.42 g/24 h) was observed in 34 patients (44%). Increased urinary excretion rates of albumin (>/=20 microgram/min), alpha1m (>/=7.0 microgram/min) or IgG (>/=5.0 microgram/min) were detected in nine (12%), nine (12%) and 11 patients (14%), respectively. Latent or overt distal renal tubular acidosis (dRTA) was observed in 18 out of 55 patients with pSS (33%). These patients had a longer duration of the disease (10+/-4 vs 8+/-4 yr; P+info)

Autosomal recessive distal renal tubular acidosis associated with Southeast Asian ovalocytosis. (3/246)

BACKGROUND: A defect in the anion exchanger 1 (AE1) of the basolateral membrane of type A intercalated cells in the renal collecting duct may result in a failure to maintain a cell-to-lumen H+ gradient, leading to distal renal tubular acidosis (dRTA). Thus, dRTA may occur in Southeast Asian ovalocytosis (SAO), a common AE1 gene abnormality observed in Southeast Asia and Melanesia. Our study investigated whether or not this renal acidification defect exists in individuals with SAO. METHODS: Short and three-day NH4Cl loading tests were performed in 20 individuals with SAO and in two subjects, including their families, with both SAO and dRTA. Mutations of AE1 gene in individuals with SAO and members of the two families were also studied. RESULTS: Renal acidification in the 20 individuals with SAO and in the parents of the two families was normal. However, the two clinically affected individuals with SAO and dRTA had compound heterozygosity of 27 bp deletion in exon 11 and missense mutation G701D resulting from a CGG-->CAG substitution in exon 17 of the AE1 gene. Red cells of the two subjects with dRTA and SAO and the family members with SAO showed an approximate 40% reduction in sulfate influx with normal 4,4'-di-isothiocyanato-stilbene-2,2'-disulfonic acid sensitivity and pH dependence. CONCLUSION: These findings suggest that compound heterozygosity of abnormal AE1 genes causes autosomal recessive dRTA in SAO.  (+info)

Localization of a gene for autosomal recessive distal renal tubular acidosis with normal hearing (rdRTA2) to 7q33-34. (4/246)

Failure of distal nephrons to excrete excess acid results in the "distal renal tubular acidoses" (dRTA). Early childhood features of autosomal recessive dRTA include severe metabolic acidosis with inappropriately alkaline urine, poor growth, rickets, and renal calcification. Progressive bilateral sensorineural hearing loss (SNHL) is evident in approximately one-third of patients. We have recently identified mutations in ATP6B1, encoding the B-subunit of the collecting-duct apical proton pump, as a cause of recessive dRTA with SNHL. We now report the results of genetic analysis of 13 kindreds with recessive dRTA and normal hearing. Analysis of linkage and molecular examination of ATP6B1 indicated that mutation in ATP6B1 rarely, if ever, accounts for this phenotype, prompting a genomewide linkage search for loci underlying this trait. The results strongly supported linkage with locus heterogeneity to a segment of 7q33-34, yielding a maximum multipoint LOD score of 8.84 with 68% of kindreds linked. The LOD-3 support interval defines a 14-cM region flanked by D7S500 and D7S688. That 4 of these 13 kindreds do not support linkage to rdRTA2 and ATP6B1 implies the existence of at least one additional dRTA locus. These findings establish that genes causing recessive dRTA with normal and impaired hearing are different, and they identify, at 7q33-34, a new locus, rdRTA2, for recessive dRTA with normal hearing.  (+info)

NH4+ secretion in inner medullary collecting duct in potassium deprivation: role of colonic H+-K+-ATPase. (5/246)

NH4+ secretion in inner medullary collecting duct in potassium deprivation: Role of colonic H+-K+-ATPase. BACKGROUND: In K+ deprivation (KD), gastric (g) H+-K+-ATPase (HKA) is suppressed, whereas colonic (c) HKA is induced in the terminal inner medullary collecting duct (IMCD). We hypothesized that in KD, cHKA is induced and can mediate the secretion of NH4+. METHODS: Rats were sacrificed after 2, 3, 6, or 14 days on regular (NML) or K+-free (KD) diet. mRNA expression of HKA isoforms in terminal inner medulla was examined and correlated with NH4+ secretion in perfused IMCD in vitro. RESULTS: Urinary NH4+ excretion increased after K+-free diet for six days. In terminal inner medulla, cHKA expression was strongly induced, whereas gHKA expression was decreased. NH4+ secretion increased by 62% in KD (JtNH4+ 0.57 vs. 0.92 pmol/min/mm tubule length, P < 0.001). Ouabain (1 mM) in perfusate inhibited NH4+ secretion in KD by 45% (P < 0.002) but not in NML. At luminal pH 7.7, which inhibits NH3 diffusion, NH4+ secretion in IMCD was 140% higher in KD (0.36 vs. 0.15, P < 0.03) and was sensitive to ouabain. ROMK-1 mRNA expression was induced in parallel with cHKA in inner medulla. CONCLUSIONS: These data suggest that in KD, cHKA replaces gHKA and mediates enhanced secretion of NH4+ (and H+) into the lumen facilitated by K+ recycling through ROMK-1.  (+info)

Study of urinary acidification in patients with idiopathic hypocitraturia. (6/246)

Hypocitraturia (HCit) is one of the most remarkable features of renal tubular acidosis, but an acidification defect is not seen in the majority of hypocitraturic patients, whose disease is denoted idiopathic hypocitraturia. In order to assess the integrity of urinary acidification mechanisms in hypocitraturic idiopathic calcium stone formers, we studied two groups of patients, hypocitraturic (HCit, N = 21, 39.5 +/- 11.5 years, 11 females and 10 males) and normocitraturic (NCit, N = 23, 40.2 +/- 11.7 years, 16 females and 7 males) subjects, during a short ammonium chloride loading test lasting 8 h. During the baseline period HCit patients showed significantly higher levels of titratable acid (TA). After the administration of ammonium chloride, mean urinary pH (3rd to 8th hour) and TA and ammonium excretion did not differ significantly between groups. Conversely, during the first hour mean urinary pH was lower and TA and ammonium excretion was higher in HCit. The enhanced TA excretion by HCit during the baseline period and during the first hour suggests that the phosphate buffer mechanism is activated. The earlier response in ammonium excretion by HCit further supports other evidence that acidification mechanisms react promptly. The present results suggest that in the course of lithiasic disease, hypocitraturia coexists with subtle changes in the excretion of hydrogen ions in basal situations.  (+info)

Hypokalaemic paralysis. (7/246)

Hypokalaemic paralysis is a relatively uncommon but potentially life-threatening clinical syndrome. If recognised and treated appropriately, patients recover without any clinical sequellae. The syndrome of hypokalaemic paralysis represents a heterogeneous group of disorders characterised clinically by hypokalaemia and acute systemic weakness. Most cases are due to familial or primary hypokalaemic periodic paralysis; sporadic cases are associated with numerous other conditions including barium poisoning, hyperthyroidism, renal disorders, certain endocrinopathies and gastrointestinal potassium losses. The age of onset, race, family history, medications, and underlying disease states can help in identifying the cause of hypokalaemic paralysis. Initial therapy of the patient with hypokalaemic paralysis includes potassium replacement and search for underlying aetiology. Further management depends on the aetiology of hypokalaemia, severity of symptoms, and duration of disease. This review presents the differential diagnosis for hypokalaemic paralysis and discusses management of the syndrome.  (+info)

Renal involvement in primary Sjogren's syndrome. (8/246)

Renal involvement was evaluated in 62 patients with primary Sjogren's syndrome, classified according to criteria proposed by The European Classification Criteria Group. Urine concentration capacity was tested using intranasal 1-desamino-8-D-arginine-vasopressin. For patients with urine pH>5.5 without metabolic acidosis (n=28), an acidification test with ammonium chloride was performed. Urinary citrate, albumin, NAG, ALP and beta2-microglobulin were measured and creatinine clearance was calculated. Maximum urine concentration capacity and creatinine clearance were reduced in 13 (21%). Albumin excretion was >30 microg/min in only one patient (1.6%). Seven patients (11.3%) had complete or incomplete distal renal tubular acidosis (dRTA), four had reduced creatinine clearance and five had reduced maximum urine concentration capacity. The ratio of citrate/creatinine in spot urine was below the 2.5 percentile in all patients with complete or incomplete dRTA. The prevalence of dRTA was lower than in previous studies. There were also few patients with signs of glomerular disease (1.6%). The use of citrate:creatinine ratio in spot urine can be a helpful method in identifying patients with complete or incomplete dRTA.  (+info)

Acidosis is a medical condition that occurs when there is an excess accumulation of acid in the body or when the body loses its ability to effectively regulate the pH level of the blood. The normal pH range of the blood is slightly alkaline, between 7.35 and 7.45. When the pH falls below 7.35, it is called acidosis.

Acidosis can be caused by various factors, including impaired kidney function, respiratory problems, diabetes, severe dehydration, alcoholism, and certain medications or toxins. There are two main types of acidosis: metabolic acidosis and respiratory acidosis.

Metabolic acidosis occurs when the body produces too much acid or is unable to eliminate it effectively. This can be caused by conditions such as diabetic ketoacidosis, lactic acidosis, kidney failure, and ingestion of certain toxins.

Respiratory acidosis, on the other hand, occurs when the lungs are unable to remove enough carbon dioxide from the body, leading to an accumulation of acid. This can be caused by conditions such as chronic obstructive pulmonary disease (COPD), asthma, and sedative overdose.

Symptoms of acidosis may include fatigue, shortness of breath, confusion, headache, rapid heartbeat, and in severe cases, coma or even death. Treatment for acidosis depends on the underlying cause and may include medications, oxygen therapy, fluid replacement, and dialysis.

Lactic acidosis is a medical condition characterized by an excess accumulation of lactic acid in the body. Lactic acid is a byproduct produced in the muscles and other tissues during periods of low oxygen supply or increased energy demand. Under normal circumstances, lactic acid is quickly metabolized and cleared from the body. However, when the production of lactic acid exceeds its clearance, it can lead to a state of acidosis, where the pH of the blood becomes too acidic.

Lactic acidosis can be caused by several factors, including:

* Prolonged exercise or strenuous physical activity
* Severe illness or infection
* Certain medications, such as metformin and isoniazid
* Alcoholism
* Hypoxia (low oxygen levels) due to lung disease, heart failure, or anemia
* Inherited metabolic disorders that affect the body's ability to metabolize lactic acid

Symptoms of lactic acidosis may include rapid breathing, fatigue, muscle weakness, nausea, vomiting, and abdominal pain. Severe cases can lead to coma, organ failure, and even death. Treatment typically involves addressing the underlying cause of the condition and providing supportive care, such as administering intravenous fluids and bicarbonate to help restore normal pH levels.

Respiratory acidosis is a medical condition that occurs when the lungs are not able to remove enough carbon dioxide (CO2) from the body, leading to an increase in the amount of CO2 in the bloodstream and a decrease in the pH of the blood. This can happen due to various reasons such as chronic lung diseases like emphysema or COPD, severe asthma attacks, neuromuscular disorders that affect breathing, or when someone is not breathing deeply or frequently enough, such as during sleep apnea or drug overdose.

Respiratory acidosis can cause symptoms such as headache, confusion, shortness of breath, and in severe cases, coma and even death. Treatment for respiratory acidosis depends on the underlying cause but may include oxygen therapy, bronchodilators, or mechanical ventilation to help support breathing.

Renal tubular acidosis (RTA) is a medical condition that occurs when the kidneys are unable to properly excrete acid into the urine, leading to an accumulation of acid in the bloodstream. This results in a state of metabolic acidosis.

There are several types of RTA, but renal tubular acidosis type 1 (also known as distal RTA) is characterized by a defect in the ability of the distal tubules to acidify the urine, leading to an inability to lower the pH of the urine below 5.5, even in the face of metabolic acidosis. This results in a persistently alkaline urine, which can lead to calcium phosphate stones and bone demineralization.

Type 1 RTA is often caused by inherited genetic defects, but it can also be acquired due to various kidney diseases, drugs, or autoimmune disorders. Symptoms of type 1 RTA may include fatigue, weakness, muscle cramps, decreased appetite, and vomiting. Treatment typically involves alkali therapy to correct the acidosis and prevent complications.

Acid-base equilibrium refers to the balance between the concentration of acids and bases in a solution, which determines its pH level. In a healthy human body, maintaining acid-base equilibrium is crucial for proper cellular function and homeostasis.

The balance is maintained by several buffering systems in the body, including the bicarbonate buffer system, which helps to regulate the pH of blood. This system involves the reaction between carbonic acid (a weak acid) and bicarbonate ions (a base) to form water and carbon dioxide.

The balance between acids and bases is carefully regulated by the body's respiratory and renal systems. The lungs control the elimination of carbon dioxide, a weak acid, through exhalation, while the kidneys regulate the excretion of hydrogen ions and the reabsorption of bicarbonate ions.

When the balance between acids and bases is disrupted, it can lead to acid-base disorders such as acidosis (excessive acidity) or alkalosis (excessive basicity). These conditions can have serious consequences on various organ systems if left untreated.

Bicarbonates, also known as sodium bicarbonate or baking soda, is a chemical compound with the formula NaHCO3. In the context of medical definitions, bicarbonates refer to the bicarbonate ion (HCO3-), which is an important buffer in the body that helps maintain normal pH levels in blood and other bodily fluids.

The balance of bicarbonate and carbonic acid in the body helps regulate the acidity or alkalinity of the blood, a condition known as pH balance. Bicarbonates are produced by the body and are also found in some foods and drinking water. They work to neutralize excess acid in the body and help maintain the normal pH range of 7.35 to 7.45.

In medical testing, bicarbonate levels may be measured as part of an electrolyte panel or as a component of arterial blood gas (ABG) analysis. Low bicarbonate levels can indicate metabolic acidosis, while high levels can indicate metabolic alkalosis. Both conditions can have serious consequences if not treated promptly and appropriately.

Hydrogen-ion concentration, also known as pH, is a measure of the acidity or basicity of a solution. It is defined as the negative logarithm (to the base 10) of the hydrogen ion activity in a solution. The standard unit of measurement is the pH unit. A pH of 7 is neutral, less than 7 is acidic, and greater than 7 is basic.

In medical terms, hydrogen-ion concentration is important for maintaining homeostasis within the body. For example, in the stomach, a high hydrogen-ion concentration (low pH) is necessary for the digestion of food. However, in other parts of the body such as blood, a high hydrogen-ion concentration can be harmful and lead to acidosis. Conversely, a low hydrogen-ion concentration (high pH) in the blood can lead to alkalosis. Both acidosis and alkalosis can have serious consequences on various organ systems if not corrected.

Sodium bicarbonate, also known as baking soda, is a chemical compound with the formula NaHCO3. It is a white solid that is crystalline but often appears as a fine powder. It has a slightly salty, alkaline taste and is commonly used in cooking as a leavening agent.

In a medical context, sodium bicarbonate is used as a medication to treat conditions caused by high levels of acid in the body, such as metabolic acidosis. It works by neutralizing the acid and turning it into a harmless salt and water. Sodium bicarbonate can be given intravenously or orally, depending on the severity of the condition being treated.

It is important to note that sodium bicarbonate should only be used under the supervision of a healthcare professional, as it can have serious side effects if not used properly. These may include fluid buildup in the body, electrolyte imbalances, and an increased risk of infection.

Alkalosis is a medical condition that refers to an excess of bases or a decrease in the concentration of hydrogen ions (H+) in the blood, leading to a higher than normal pH level. The normal range for blood pH is typically between 7.35 and 7.45. A pH above 7.45 indicates alkalosis.

Alkalosis can be caused by several factors, including:

1. Metabolic alkalosis: This type of alkalosis occurs due to an excess of bicarbonate (HCO3-) in the body, which can result from conditions such as excessive vomiting, hyperventilation, or the use of certain medications like diuretics.
2. Respiratory alkalosis: This form of alkalosis is caused by a decrease in carbon dioxide (CO2) levels in the blood due to hyperventilation or other conditions that affect breathing, such as high altitude, anxiety, or lung disease.

Symptoms of alkalosis can vary depending on its severity and underlying cause. Mild alkalosis may not produce any noticeable symptoms, while severe cases can lead to muscle twitching, cramps, tremors, confusion, and even seizures. Treatment for alkalosis typically involves addressing the underlying cause and restoring the body's normal pH balance through medications or other interventions as necessary.

Ammonium chloride is an inorganic compound with the formula NH4Cl. It is a white crystalline salt that is highly soluble in water and can be produced by combining ammonia (NH3) with hydrochloric acid (HCl). Ammonium chloride is commonly used as a source of hydrogen ions in chemical reactions, and it has a variety of industrial and medical applications.

In the medical field, ammonium chloride is sometimes used as a expectorant to help thin and loosen mucus in the respiratory tract, making it easier to cough up and clear from the lungs. It may also be used to treat conditions such as metabolic alkalosis, a condition characterized by an excess of base in the body that can lead to symptoms such as confusion, muscle twitching, and irregular heartbeat.

However, it is important to note that ammonium chloride can have side effects, including stomach upset, nausea, vomiting, and diarrhea. It should be used under the guidance of a healthcare professional and should not be taken in large amounts or for extended periods of time without medical supervision.

Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes (MELAS) syndrome is a rare inherited mitochondrial disorder that affects the body's energy production mechanisms. It is characterized by a combination of symptoms including recurrent headaches, vomiting, seizures, vision loss, hearing impairment, muscle weakness, and stroke-like episodes affecting primarily young adults.

The condition is caused by mutations in the mitochondrial DNA (mtDNA), most commonly the A3243G point mutation in the MT-TL1 gene. The symptoms of MELAS syndrome can vary widely among affected individuals, even within the same family, due to the complex inheritance pattern of mtDNA.

MELAS syndrome is typically diagnosed based on a combination of clinical features, laboratory tests, and genetic testing. Treatment is supportive and aimed at managing individual symptoms as they arise.

Carbon dioxide (CO2) is a colorless, odorless gas that is naturally present in the Earth's atmosphere. It is a normal byproduct of cellular respiration in humans, animals, and plants, and is also produced through the combustion of fossil fuels such as coal, oil, and natural gas.

In medical terms, carbon dioxide is often used as a respiratory stimulant and to maintain the pH balance of blood. It is also used during certain medical procedures, such as laparoscopic surgery, to insufflate (inflate) the abdominal cavity and create a working space for the surgeon.

Elevated levels of carbon dioxide in the body can lead to respiratory acidosis, a condition characterized by an increased concentration of carbon dioxide in the blood and a decrease in pH. This can occur in conditions such as chronic obstructive pulmonary disease (COPD), asthma, or other lung diseases that impair breathing and gas exchange. Symptoms of respiratory acidosis may include shortness of breath, confusion, headache, and in severe cases, coma or death.

An acid-base imbalance refers to a disturbance in the normal balance of acids and bases in the body, which can lead to serious health consequences. The body maintains a delicate balance between acids and bases, which is measured by the pH level of the blood. The normal range for blood pH is between 7.35 and 7.45, with a pH below 7.35 considered acidic and a pH above 7.45 considered basic or alkaline.

Acid-base imbalances can occur due to various factors such as lung or kidney disease, diabetes, severe infections, certain medications, and exposure to toxins. The two main types of acid-base imbalances are acidosis (excess acid in the body) and alkalosis (excess base in the body).

Acidosis can be further classified into respiratory acidosis (caused by impaired lung function or breathing difficulties) and metabolic acidosis (caused by an accumulation of acid in the body due to impaired kidney function, diabetes, or other conditions).

Alkalosis can also be classified into respiratory alkalosis (caused by hyperventilation or excessive breathing) and metabolic alkalosis (caused by excessive loss of stomach acid or an excess intake of base-forming substances).

Symptoms of acid-base imbalances may include confusion, lethargy, shortness of breath, rapid heartbeat, nausea, vomiting, and muscle weakness. If left untreated, these conditions can lead to serious complications such as coma, seizures, or even death. Treatment typically involves addressing the underlying cause of the imbalance and may include medications, oxygen therapy, or fluid and electrolyte replacement.

Diabetic ketoacidosis (DKA) is a serious metabolic complication characterized by the triad of hyperglycemia, metabolic acidosis, and increased ketone bodies. It primarily occurs in individuals with diabetes mellitus type 1, but it can also be seen in some people with diabetes mellitus type 2, particularly during severe illness or surgery.

The condition arises when there is a significant lack of insulin in the body, which impairs the ability of cells to take up glucose for energy production. As a result, the body starts breaking down fatty acids to produce energy, leading to an increase in ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) in the bloodstream. This process is called ketosis.

In DKA, the excessive production of ketone bodies results in metabolic acidosis, which is characterized by a lower than normal pH level in the blood (< 7.35) and an elevated serum bicarbonate level (< 18 mEq/L). The hyperglycemia in DKA is due to both increased glucose production and decreased glucose utilization by cells, which can lead to severe dehydration and electrolyte imbalances.

Symptoms of diabetic ketoacidosis include excessive thirst, frequent urination, nausea, vomiting, abdominal pain, fatigue, fruity breath odor, and altered mental status. If left untreated, DKA can progress to coma and even lead to death. Treatment typically involves administering insulin, fluid replacement, and electrolyte management in a hospital setting.

Lactates, also known as lactic acid, are compounds that are produced by muscles during intense exercise or other conditions of low oxygen supply. They are formed from the breakdown of glucose in the absence of adequate oxygen to complete the full process of cellular respiration. This results in the production of lactate and a hydrogen ion, which can lead to a decrease in pH and muscle fatigue.

In a medical context, lactates may be measured in the blood as an indicator of tissue oxygenation and metabolic status. Elevated levels of lactate in the blood, known as lactic acidosis, can indicate poor tissue perfusion or hypoxia, and may be seen in conditions such as sepsis, cardiac arrest, and severe shock. It is important to note that lactates are not the primary cause of acidemia (low pH) in lactic acidosis, but rather a marker of the underlying process.

Hypercapnia is a state of increased carbon dioxide (CO2) concentration in the blood, typically defined as an arterial CO2 tension (PaCO2) above 45 mmHg. It is often associated with conditions that impair gas exchange or eliminate CO2 from the body, such as chronic obstructive pulmonary disease (COPD), severe asthma, respiratory failure, or certain neuromuscular disorders. Hypercapnia can cause symptoms such as headache, confusion, shortness of breath, and in severe cases, it can lead to life-threatening complications such as respiratory acidosis, coma, and even death if not promptly treated.

Respiratory alkalosis is a medical condition that occurs when there is an excess base (bicarbonate) and/or a decrease in carbon dioxide in the body. This leads to an increase in pH level of the blood, making it more alkaline than normal. Respiratory alkalosis is usually caused by conditions that result in hyperventilation, such as anxiety, lung disease, or high altitude. It can also be caused by certain medications and medical procedures. Symptoms of respiratory alkalosis may include lightheadedness, confusion, and tingling in the fingers and toes. Treatment typically involves addressing the underlying cause of the condition.

Lactic acid, also known as 2-hydroxypropanoic acid, is a chemical compound that plays a significant role in various biological processes. In the context of medicine and biochemistry, lactic acid is primarily discussed in relation to muscle metabolism and cellular energy production. Here's a medical definition for lactic acid:

Lactic acid (LA): A carboxylic acid with the molecular formula C3H6O3 that plays a crucial role in anaerobic respiration, particularly during strenuous exercise or conditions of reduced oxygen availability. It is formed through the conversion of pyruvate, catalyzed by the enzyme lactate dehydrogenase (LDH), when there is insufficient oxygen to complete the final step of cellular respiration in the Krebs cycle. The accumulation of lactic acid can lead to acidosis and muscle fatigue. Additionally, lactic acid serves as a vital intermediary in various metabolic pathways and is involved in the production of glucose through gluconeogenesis in the liver.

Blood gas analysis is a medical test that measures the levels of oxygen and carbon dioxide in the blood, as well as the pH level, which indicates the acidity or alkalinity of the blood. This test is often used to evaluate lung function, respiratory disorders, and acid-base balance in the body. It can also be used to monitor the effectiveness of treatments for conditions such as chronic obstructive pulmonary disease (COPD), asthma, and other respiratory illnesses. The analysis is typically performed on a sample of arterial blood, although venous blood may also be used in some cases.

Potassium citrate is a medication and dietary supplement that contains potassium and citrate. Medically, it is used to treat and prevent kidney stones, as well as to manage metabolic acidosis in people with chronic kidney disease. Potassium citrate works by increasing the pH of urine, making it less acidic, which can help to dissolve certain types of kidney stones and prevent new ones from forming. It is also used as an alkalizing agent in the treatment of various conditions that cause acidosis.

In addition to its medical uses, potassium citrate is also found naturally in some fruits and vegetables, such as oranges, grapefruits, lemons, limes, and spinach. It is often used as a food additive and preservative, and can be found in a variety of processed foods and beverages.

It's important to note that taking too much potassium citrate can lead to high levels of potassium in the blood, which can be dangerous. Therefore, it is important to follow the dosage instructions carefully and talk to your doctor before taking this medication if you have any medical conditions or are taking any other medications.

Phenformin is a medication that was previously used to treat type 2 diabetes. It belongs to a class of drugs called biguanides, which work to decrease the amount of glucose produced by the liver and increase the body's sensitivity to insulin. However, phenformin was associated with an increased risk of lactic acidosis, a potentially life-threatening condition characterized by an excessive buildup of lactic acid in the bloodstream. As a result, it is no longer available or recommended for use in most countries, including the United States.

A Sodium-Hydrogen Antiporter (NHA) is a type of membrane transport protein that exchanges sodium ions (Na+) and protons (H+) across a biological membrane. It is also known as a Na+/H+ antiporter or exchanger. This exchange mechanism plays a crucial role in regulating pH, cell volume, and intracellular sodium concentration within various cells and organelles, including the kidney, brain, heart, and mitochondria.

In general, NHA transporters utilize the energy generated by the electrochemical gradient of sodium ions across a membrane to drive the uphill transport of protons from inside to outside the cell or organelle. This process helps maintain an optimal intracellular pH and volume, which is essential for proper cellular function and homeostasis.

There are several isoforms of Sodium-Hydrogen Antiporters found in different tissues and organelles, each with distinct physiological roles and regulatory mechanisms. Dysfunction or alterations in NHA activity have been implicated in various pathophysiological conditions, such as hypertension, heart failure, neurological disorders, and cancer.

Ammonia is a colorless, pungent-smelling gas with the chemical formula NH3. It is a compound of nitrogen and hydrogen and is a basic compound, meaning it has a pH greater than 7. Ammonia is naturally found in the environment and is produced by the breakdown of organic matter, such as animal waste and decomposing plants. In the medical field, ammonia is most commonly discussed in relation to its role in human metabolism and its potential toxicity.

In the body, ammonia is produced as a byproduct of protein metabolism and is typically converted to urea in the liver and excreted in the urine. However, if the liver is not functioning properly or if there is an excess of protein in the diet, ammonia can accumulate in the blood and cause a condition called hyperammonemia. Hyperammonemia can lead to serious neurological symptoms, such as confusion, seizures, and coma, and is treated by lowering the level of ammonia in the blood through medications, dietary changes, and dialysis.

Sodium-bicarbonate symporters, also known as sodium bicarbonate co-transporters, are membrane transport proteins that facilitate the movement of both sodium ions (Na+) and bicarbonate ions (HCO3-) across the cell membrane in the same direction. These transporters play a crucial role in maintaining acid-base balance in the body by regulating the concentration of bicarbonate ions, which is an important buffer in the blood and other bodily fluids.

The term "symporter" refers to the fact that these proteins transport two or more different molecules or ions in the same direction across a membrane. In this case, sodium-bicarbonate symporters co-transport one sodium ion and one bicarbonate ion together, usually using a concentration gradient of sodium to drive the uptake of bicarbonate.

These transporters are widely expressed in various tissues, including the kidneys, where they help reabsorb bicarbonate ions from the urine back into the bloodstream, and the gastrointestinal tract, where they contribute to the absorption of sodium and bicarbonate from food and drink. Dysfunction of sodium-bicarbonate symporters has been implicated in several diseases, including renal tubular acidosis and hypertension.

In medical terms, acids refer to a class of chemicals that have a pH less than 7 and can donate protons (hydrogen ions) in chemical reactions. In the context of human health, acids are an important part of various bodily functions, such as digestion. However, an imbalance in acid levels can lead to medical conditions. For example, an excess of hydrochloric acid in the stomach can cause gastritis or peptic ulcers, while an accumulation of lactic acid due to strenuous exercise or decreased blood flow can lead to muscle fatigue and pain.

Additionally, in clinical laboratory tests, certain substances may be tested for their "acidity" or "alkalinity," which is measured using a pH scale. This information can help diagnose various medical conditions, such as kidney disease or diabetes.

Hydrochloric acid, also known as muriatic acid, is not a substance that is typically found within the human body. It is a strong mineral acid with the chemical formula HCl. In a medical context, it might be mentioned in relation to gastric acid, which helps digest food in the stomach. Gastric acid is composed of hydrochloric acid, potassium chloride and sodium chloride dissolved in water. The pH of hydrochloric acid is very low (1-2) due to its high concentration of H+ ions, making it a strong acid. However, it's important to note that the term 'hydrochloric acid' does not directly refer to a component of human bodily fluids or tissues.

Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.

Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.

Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.

Hyperkalemia is a medical condition characterized by an elevated level of potassium (K+) in the blood serum, specifically when the concentration exceeds 5.0-5.5 mEq/L (milliequivalents per liter). Potassium is a crucial intracellular ion that plays a significant role in various physiological processes, including nerve impulse transmission, muscle contraction, and heart rhythm regulation.

Mild to moderate hyperkalemia might not cause noticeable symptoms but can still have harmful effects on the body, particularly on the cardiovascular system. Severe cases of hyperkalemia (potassium levels > 6.5 mEq/L) can lead to potentially life-threatening arrhythmias and heart failure.

Hyperkalemia may result from various factors, such as kidney dysfunction, hormonal imbalances, medication side effects, trauma, or excessive potassium intake. Prompt identification and management of hyperkalemia are essential to prevent severe complications and ensure proper treatment.

Fanconi syndrome is a medical condition that affects the proximal tubules of the kidneys. These tubules are responsible for reabsorbing various substances, such as glucose, amino acids, and electrolytes, back into the bloodstream after they have been filtered through the kidneys.

In Fanconi syndrome, there is a defect in the reabsorption process, causing these substances to be lost in the urine instead. This can lead to a variety of symptoms, including:

* Polyuria (excessive urination)
* Polydipsia (excessive thirst)
* Dehydration
* Metabolic acidosis (an imbalance of acid and base in the body)
* Hypokalemia (low potassium levels)
* Hypophosphatemia (low phosphate levels)
* Vitamin D deficiency
* Rickets (softening and weakening of bones in children) or osteomalacia (softening of bones in adults)

Fanconi syndrome can be caused by a variety of underlying conditions, including genetic disorders, kidney diseases, drug toxicity, and heavy metal poisoning. Treatment typically involves addressing the underlying cause, as well as managing symptoms such as electrolyte imbalances and acid-base disturbances.

A transfer RNA (tRNA) molecule that carries the amino acid leucine is referred to as "tRNA-Leu." This specific tRNA molecule recognizes and binds to a codon (a sequence of three nucleotides in mRNA) during protein synthesis or translation. In this case, tRNA-Leu can recognize and pair with any of the following codons: UUA, UUG, CUU, CUC, CUA, and CUG. Once bound to the mRNA at the ribosome, leucine is added to the growing polypeptide chain through the action of aminoacyl-tRNA synthetase enzymes that catalyze the attachment of specific amino acids to their corresponding tRNAs. This ensures the accurate and efficient production of proteins based on genetic information encoded in mRNA.

Acid-sensing ion channels (ASICs) are a type of ion channel protein found in nerve cells (neurons) that are activated by acidic environments. They are composed of homomeric or heteromeric combinations of six different subunits, designated ASIC1a, ASIC1b, ASIC2a, ASIC2b, ASIC3, and ASIC4. These channels play important roles in various physiological processes, including pH homeostasis, nociception (pain perception), and mechanosensation (the ability to sense mechanical stimuli).

ASICs are permeable to both sodium (Na+) and calcium (Ca2+) ions. When the extracellular pH decreases, the channels open, allowing Na+ and Ca2+ ions to flow into the neuron. This influx of cations can depolarize the neuronal membrane, leading to the generation of action potentials and neurotransmitter release.

In the context of pain perception, ASICs are activated by the acidic environment in damaged tissues or ischemic conditions, contributing to the sensation of pain. In addition, some ASIC subunits have been implicated in synaptic plasticity, learning, and memory processes. Dysregulation of ASIC function has been associated with various pathological conditions, including neuropathic pain, ischemia, epilepsy, and neurodegenerative diseases.

In the context of medicine, and specifically in physiology and respiratory therapy, partial pressure (P or p) is a measure of the pressure exerted by an individual gas in a mixture of gases. It's commonly used to describe the concentrations of gases in the body, such as oxygen (PO2), carbon dioxide (PCO2), and nitrogen (PN2).

The partial pressure of a specific gas is calculated as the fraction of that gas in the total mixture multiplied by the total pressure of the mixture. This concept is based on Dalton's law, which states that the total pressure exerted by a mixture of gases is equal to the sum of the pressures exerted by each individual gas.

For example, in room air at sea level, the partial pressure of oxygen (PO2) is approximately 160 mmHg (mm of mercury), which represents about 21% of the total barometric pressure (760 mmHg). This concept is crucial for understanding gas exchange in the lungs and how gases move across membranes, such as from alveoli to blood and vice versa.

Glutaminase is an enzyme that catalyzes the conversion of L-glutamine, which is a type of amino acid, into glutamate and ammonia. This reaction is an essential part of nitrogen metabolism in many organisms, including humans. There are several forms of glutaminase found in different parts of the body, with varying properties and functions.

In humans, there are two major types of glutaminase: mitochondrial and cytosolic. Mitochondrial glutaminase is primarily found in the kidneys and brain, where it plays a crucial role in energy metabolism by converting glutamine into glutamate, which can then be further metabolized to produce ATP (adenosine triphosphate), a major source of cellular energy.

Cytosolic glutaminase, on the other hand, is found in many tissues throughout the body and is involved in various metabolic processes, including nucleotide synthesis and protein degradation.

Glutaminase activity has been implicated in several disease states, including cancer, where some tumors have been shown to have elevated levels of glutaminase expression, allowing them to use glutamine as a major source of energy and growth. Inhibitors of glutaminase are currently being investigated as potential therapeutic agents for the treatment of cancer.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Dichloroacetic acid (DCA) is a chemical compound with the formula CCl2CO2H. It is a colorless liquid that is used as a reagent in organic synthesis and as a laboratory research tool. DCA is also a byproduct of water chlorination and has been found to occur in low levels in some chlorinated drinking waters.

In the medical field, DCA has been studied for its potential anticancer effects. Preclinical studies have suggested that DCA may be able to selectively kill cancer cells by inhibiting the activity of certain enzymes involved in cell metabolism. However, more research is needed to determine whether DCA is safe and effective as a cancer treatment in humans.

It is important to note that DCA is not currently approved by regulatory agencies such as the U.S. Food and Drug Administration (FDA) for use as a cancer treatment. It should only be used in clinical trials or under the supervision of a qualified healthcare professional.

Nephrocalcinosis is a medical condition characterized by the deposition of calcium salts in the renal parenchyma, specifically within the tubular epithelial cells and interstitium of the kidneys. This process can lead to chronic inflammation, tissue damage, and ultimately impaired renal function if left untreated.

The condition is often associated with metabolic disorders such as hyperparathyroidism, distal renal tubular acidosis, or hyperoxaluria; medications like loop diuretics, corticosteroids, or calcineurin inhibitors; and chronic kidney diseases. The diagnosis of nephrocalcinosis is typically made through imaging studies such as ultrasound, CT scan, or X-ray. Treatment usually involves addressing the underlying cause, modifying dietary habits, and administering medications to control calcium levels in the body.

The rumen is the largest compartment of the stomach in ruminant animals, such as cows, goats, and sheep. It is a specialized fermentation chamber where microbes break down tough plant material into nutrients that the animal can absorb and use for energy and growth. The rumen contains billions of microorganisms, including bacteria, protozoa, and fungi, which help to break down cellulose and other complex carbohydrates in the plant material through fermentation.

The rumen is characterized by its large size, muscular walls, and the presence of a thick mat of partially digested food and microbes called the rumen mat or cud. The animal regurgitates the rumen contents periodically to chew it again, which helps to break down the plant material further and mix it with saliva, creating a more favorable environment for fermentation.

The rumen plays an essential role in the digestion and nutrition of ruminant animals, allowing them to thrive on a diet of low-quality plant material that would be difficult for other animals to digest.

... (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the ... In a large Asian series of Distal renal Tubular Acidosis in Sjogren's Syndrome, late diagnosis is a rule in spite of overt ... It was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic ... Bianic F, Guelfucci F, Robin L, Martre C, Game D, Bockenhauer D (2021). "Epidemiology of Distal Renal Tubular Acidosis: A Study ...
... (pRTA) or type 2 renal tubular acidosis (RTA) is a type of RTA caused by a failure of the ... Renal tubular acidosis Distal renal tubular acidosis Rodriguez Soriano J, Boichis H, Stark H, Edelmann CM (1967). "Proximal ... "Adult Fanconi's syndrome with renal tubular acidosis in association with renal amyloidosis: occurrence in a patient with ... Since in proximal renal tubular acidosis patients the nephron is unable to reabsorb bicarbonate, the level of bicarbonate is ...
Renal tubular acidosis Proximal renal tubular acidosis Ifosfamide "Osmosis: Renal tubular acidosis". Osmosis. Archived from the ... Distal renal tubular acidosis (dRTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a ... 1997). "Familial distal renal tubular acidosis is associated with mutations in the red cell anion exchanger (Band 3, AE1) gene ... 2000). "Band 3 mutations, renal tubular acidosis and South-East Asian ovalocytosis in Malaysia and Papua New Guinea: loss of up ...
The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis ... Rodriguez Soriano J, Boichis H, Stark H, Edelmann CM (1967). "Proximal renal tubular acidosis. A defect in bicarbonate ... Secondary hyperaldosteronism can also be caused by proximal renal tubular acidosis Secondary hyperaldosteronism can also be a ... Another is renal artery stenosis, in which the reduced blood supply across the juxtaglomerular apparatus stimulates the ...
The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis ... Bailey & Love's/25th/1296 National Endocrine and Metabolic Diseases Information Service (2008). "Renal Tubular Acidosis (NIH ... such as distal renal tubular acidosis, Dent's disease, hyperparathyroidism, primary hyperoxaluria, or medullary sponge kidney. ... However, no renal tubular damage or visible deposition of calcium oxalate crystals in kidneys was found in yearling wether ...
Karet, Fiona E. (February 2009). "Mechanisms in Hyperkalemic Renal Tubular Acidosis: Figure 1". Journal of the American Society ... However, in respiratory acidosis or organic acidosis such as lactic acidosis, the effect on serum potassium are much less ... Type IV renal tubular acidosis (aldosterone resistance of the kidney's tubules) Gordon's syndrome (pseudohypoaldosteronism type ... Metabolic acidosis can cause hyperkalemia as the elevated hydrogen ions in the cells can displace potassium, causing the ...
Kashoor I, Batlle D (September 2019). "Proximal renal tubular acidosis with and without Fanconi syndrome". Kidney Research and ...
... is a neonatal form of renal tubular acidosis. It is characterized by distal renal tubular acidosis ... This, along with the inability to excrete other acids in the body, contribute to metabolic acidosis and renal tubular acidosis ... Fanconi G (February 1954). "Tubular Insufficiency and Renal Dwarfism". Archives of Disease in Childhood. 29 (143): 1-6. doi: ... Laboratory findings can include metabolic acidosis, hyperchloremia, hypercalcemia, and elevated urinary pH. Specifically, the ...
... distal renal tubular acidosis, and Southeast Asian ovalocytosis". Kidney International. 62 (1): 10-19. doi:10.1046/j.1523- ...
Manz F, Schärer K, Janka P, Lombeck J (1978). "Renal magnesium wasting, incomplete tubular acidosis, hypercalciuria and ... Defects in this gene are a cause of primary hypomagnesemia, which is characterized by massive renal magnesium wasting with ... a renal tight junction protein required for paracellular Mg2+ resorption". Science. 285 (5424): 103-6. doi:10.1126/science. ...
Other mutations disrupt kidney bicarbonate transport and cause proximal renal tubular acidosis. NBCe1-A aka kNBC1 (mainly ... 1999). "Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalities". Nat. Genet. 23 ... "Topological location and structural importance of the NBCe1-A residues mutated in proximal renal tubular acidosis". J. Biol. ... 2003). "Localization of NBC-1 variants in human kidney and renal cell carcinoma". Biochem. Biophys. Res. Commun. 310 (4): 1213- ...
Known for Lightwood-Albright syndrome, a neonatal form of renal tubular acidosis. In 1941 Albright was elected a Fellow of the ... and renal tubular acidosis (inability of the kidneys to regulate the acid-base balance in the body), and recognized the ...
Defects in this enzyme are associated with osteopetrosis and renal tubular acidosis. Renal carbonic anhydrase allows the ... Carbonic anhydrase II deficiency syndrome (osteopetrosis associated with renal tubular acidosis and cerebral calcification)". ... recessive osteopetrosis with renal tubular acidosis and cerebral calcification". Pediatrics. 77 (3): 371-81. doi:10.1542/peds. ...
This results in disruptions of renal reabsorption. Examples of these disorders include Iminoglycinuria, renal tubular acidosis ... Inborn errors of renal tubular transport are metabolic disorders which lead to impairment in the ability of solutes, such as ... salts or amino acids, to be transported across the brush border of the renal tubule. ...
A key insight was that in the group of diseases termed 'Renal Tubular Acidosis' (RTA), urinary excretion of ammonium was ... 2012). "Tropical distal renal tubular acidosis: clinical and epidemiological studies in 78 patients". QJM. 105 (9): 861-877. ... 2012). "Tropical distal renal tubular acidosis: clinical and epidemiological studies in 78 patients". QJM. 105 (9): 861-877. ... Unwin, RJ (2012). "Back to the future: renal tubular acidosis then and now". QJM. 105 (9): 915-916. doi:10.1093/qjmed/hcs134. ...
"Entrez Gene: ATP6V1B1 ATPase, H+ transporting, lysosomal 56/58kDa, V1 subunit B1 (Renal tubular acidosis with deafness)". Human ... Mutations in this gene cause distal renal tubular acidosis associated with sensorineural deafness. GRCh38: Ensembl release 89: ... "Mutations in the gene encoding B1 subunit of H+-ATPase cause renal tubular acidosis with sensorineural deafness". Nat Genet. 21 ...
The loss of bicarbonate results in type 2 or proximal renal tubular acidosis. The loss of phosphate results in the bone ... The clinical features of proximal renal tubular acidosis are:[citation needed] Polyuria, polydipsia and dehydration ... renal tubular acidosis in a patient with primary Sjögren's syndrome with monoclonal gammopathy of undetermined significance". ... Growth failure Acidosis Hypokalemia Hyperchloremia Other features of the generalized proximal tubular dysfunction of the ...
LIGHTWOOD, R.; PAYNE, W. W.; BLACK, J. A. (1 December 1953). "Infantile Renal Acidosis". Pediatrics. American Academy of ... Payne, Wilfrid W. (1956). "Renal tubular defects in childhood". Pediatrics. American Academy of Pediatrics. 17 (1): 84-92. ISSN ... "Wilfrid Walter Payne". The Renal Association. Renal Association. Retrieved 27 June 2018. "Wilfrid Walter Payne". Munks Roll - ...
In 2007 the renal tubular acidosis was another clinical complication described in only one case report of two brothers with ... 2007) "Sibling cases of Vici syndrome: sleep abnormalities and complications of renal tubular acidosis". Am J Med Genet A 143(2 ... Renal abnormalities (15%) Infections of the gastrointestinal and urinary tracts are common. Swallowing and feeding difficulties ...
... citrate is used to treat a kidney stone condition called renal tubular acidosis. Potassium, in the form of potassium ... Renal handling of potassium is closely connected to sodium handling. Potassium is the major cation (positive ion) inside animal ... Since only 1-10 mg of sodium and 1-4 mg of potassium are likely to be replaced by diet, renal filtering must efficiently ... Sodium pumps in the renal tubules operate to reabsorb sodium. Potassium must be conserved, but because the amount of potassium ...
These can include "Noonan Syndrome 9," "Distal Renal Tubular Acidosis," and "Noonan Syndrome 3.". ATP6V1G2 may be involved in ... and their evaluation in autosomal recessive distal renal tubular acidosis". Gene. 297 (1-2): 169-177. doi:10.1016/S0378-1119(02 ...
Boettger T, Hübner CA, Maier H, Rust MB, Beck FX, Jentsch TJ (April 2002). "Deafness and renal tubular acidosis in mice lacking ...
Mutations in this gene are associated with renal tubular acidosis associated with preserved hearing. ATP6V0A4 has been shown to ... cause recessive distal renal tubular acidosis with preserved hearing". Nat. Genet. 26 (1): 71-5. doi:10.1038/79208. PMID ... "Localization of a gene for autosomal recessive distal renal tubular acidosis with normal hearing (rdRTA2) to 7q33-34". Am. J. ...
Deafness and renal tubular acidosis in mice lacking the K-Cl co-transporter Kcc4. Nature, 416(6883), 874-878. https://doi.org/ ...
For example, severe hypokalaemia has been associated with distal renal tubular acidosis from laxative abuse. Metabolic ... Copeland PM; Molina, H.; Ohye, Ch.; MacIas, R.; Alaminos, A.; Alvarez, L.; Teijeiro, J.; Muñoz, J.; Ortega, I. (1994). "Renal ... Wright LF, DuVal JW (1987). "Renal injury associated with laxative abuse". South Med J. 80 (10): 1304-6. doi:10.1097/00007611- ...
... may also cause a normal anion gap acidosis, specifically renal tubular acidosis type 2. "Ifosfamide". The American ...
A rare exception is a case of renal tubular acidosis purportedly caused by expired tetracycline. A study conducted by the U.S. ...
Renal tubular acidosis, hypophosphatemia and aminoaciduria. Cardiomyopathy, neurologic and dermatologic manifestations are also ... SA can function to inhibit renal tubular function, the synthesis of heme, and the immune system. The accumulation of ... The inability of cells to process tyrosine can lead to chronic liver damage ending in liver failure, as well as renal disease ... Kidney failure is a potential result of impaired kidney function, but the most common symptom associated with renal dysfunction ...
A rare exception is a case of renal tubular acidosis purportedly caused by expired tetracycline. A study conducted by the U.S. ...
... hypertension and systemic acidosis without renal failure associated with a tubular defect in potassium excretion". The American ... Renal Physiology. 305 (1): F31-41. doi:10.1152/ajprenal.00652.2012. PMC 3725674. PMID 23594824. Ring AM, Leng Q, Rinehart J, ... Renal Physiology. 290 (6): F1305-14. doi:10.1152/ajprenal.00391.2005. PMID 16403833. Jiang Y, Ferguson WB, Peng JB (February ... Renal Physiology. 304 (1): F8-F18. doi:10.1152/ajprenal.00284.2012. PMC 3543615. PMID 23054253. San-Cristobal P, Pacheco- ...
Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the ... In a large Asian series of Distal renal Tubular Acidosis in Sjogrens Syndrome, late diagnosis is a rule in spite of overt ... It was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic ... Bianic F, Guelfucci F, Robin L, Martre C, Game D, Bockenhauer D (2021). "Epidemiology of Distal Renal Tubular Acidosis: A Study ...
... renal) problems and hearing loss. Explore symptoms, inheritance, genetics of this condition. ... Renal tubular acidosis with deafness is a disorder characterized by kidney ( ... Renal tubular acidosis with progressive nerve deafness. *Renal tubular acidosis, autosomal recessive, with progressive nerve ... medlineplus.gov/genetics/condition/renal-tubular-acidosis-with-deafness/ Renal tubular acidosis with deafness. ...
Distal Renal Tubular Acidosis (dRTA) Market to register enormous growth at a significant CAGR by 2032. Several key companies ...
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Background: Normal anion gap metabolic acidosis is a common but often misdiagnosed clinical condition associated with diarrhea ... Renal Tubular Acidosis. There are three major forms of RTA: proximal RTA (type 2), distal RTA (type 1), and hyperkalemic RTA ( ... Wrong O: Distal renal tubular acidosis: the value of urinary pH, PCO2 and NH4+ measurements. Pediatr Nephrol 1991;5:249-255. ... The classification of renal tubular acidosis (RTA) may also be confusing as the defect in the proximal and distal tubules is ...
Distal renal tubular acidosis. RTA is a term applied to several clinical syndromes of metabolic acidosis that result from ... Distal renal tubular acidosis. Potassium citrate is administered in large doses, as the goal is to raise the serum bicarbonate ... A history of systemic disease, such as renal tubular acidosis, is another important consideration. ... such as primary hyperparathyroidism or renal tubular acidosis. ... Type I renal tubular acidosis. Complete type I RTA is ...
Renal Tubular Acidosis - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - Medical ... see table Some Features of Different Types of Renal Tubular Acidosis Some Features of Different Types of Renal Tubular Acidosis ... Renal tubular acidosis (RTA) is acidosis and electrolyte disturbances due to impaired renal hydrogen ion excretion (type 1), ... Renal tubular acidosis is a class of disorders in which excretion of hydrogen ions or reabsorption of filtered bicarbonate is ...
We present a case of AmBisome associated kidney injury with delayed onset of renal tubular acidosis. ... decreased renal function and hypokalemia. Liposomal Amphotericin B (AmBisome) is suggested to be associated with less ... Conventional form of Amphotericin B has been associated with renal tubular acidosis, ... Conventional form of Amphotericin B has been associated with renal tubular acidosis, decreased renal function and hypokalemia.1 ...
Case Reports 2016; 37(3): 169-173 PubMed PMID: 27179580 Keywords: Acidosis, Renal Tubular:complications, Adult, DNA:immunology ... Systemic lupus erythematosus and renal tubular acidosis associated with hyperthyroidism. Case Report.. Deng D, Sun L, Xia T, Xu ... Deng D, Sun L, Xia T, Xu M, Wang Y, Zhang Q. Systemic lupus erythematosus and renal tubular acidosis associated with ...
Learn how it can cause unexplained hypokalaemia and metabolic acidosis in young patients. Increase your awareness as an ... E. J. F. Carlisle, S. M. Donnelly, et al., "Glue-Sniffing and Distal Renal Tubular Acidosis: Sticking to the Facts," Journal of ... D. C. Batlle, S. Sabatini and N. A. Kurtzman, "On the Mechanism of Toluene-Induced Renal Tubular Acidosis," Nephron, Vol. 49, ... J.-J Hong, J.-L Lin, et al., "Chronic Glue Sniffer with Hy perchloraemia Metabolic Acidosis, Rhabdomyolysis, Irreversible ...
... renal osteodystrophy, Fanconi syndrome), tumor-induced osteomalacia, hypophosphatasia, McCune-Albright syndrome, and ... Renal tubular acidosis, through phosphate wasting, may also cause rickets.. Renal osteodystrophy. In end-stage renal disease, ... Renal Causes. Fanconi syndrome. Fanconi syndrome is a disorder of proximal renal tubular transport. Phosphate, amino acid, ... In addition, a renal tubular defect that reduces reabsorption may alter phosphate metabolism. Finally, a genetic absence of the ...
Renal tubular acidosis, glomerulonephritis, myoglobinuria, and renal failure have been observed (Poisondex, 2014). ... In solvent abusers, electrolyte and acid-base disturbances have resulted in renal tubular acidosis, deficiency of potassium, ... Disorders of the muscles, cardiovascular effects, renal tubular damage, and sudden death have occurred in chronic abusers of ... Renal. Blood and protein in the urine can occur after massive inhalation. These effects are usually reversible if exposure is ...
Renal tubular acidosis and hypokalaemia may occur following acute overdose and in patients taking ibuprofen products over long ... Renal tubular acidosis and hypokalaemia have been reported in the post-marketing setting typically following prolonged use of ... Prolonged use at higher than recommended doses may result in severe hypokalaemia and renal tubular acidosis. Symptoms may ... Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal ...
Acidosis, Renal Tubular. *Corneal Edema. *Dehydration. *Drug Overdose. *Drug Toxicity. *Dry Eye Syndromes ...
... renal tubular acidosis, and mitochondrial disease.. #Hypogammaglobulinemia. ...
Case reports: Unusual association between renal tubular acidosis and Chilaiditi syndrome: a case report. N. Younes and M. Sbeih ... Effect of menopause and renal function on vitamin D status in Iranian women. G.R. Omrani, S.M. Masoompour, A. Sadegholvaad and ...
Renal: If untreated, the proximal renal tubular acidosis leads to failure to thrive and metabolic collapse. By the second to ... Topaloglu R, Ludwig M, Çelebi Tayfur A. Selective proximal renal tubular involvement and dyslipidemia in two cousins with ... and renal tubular dysfunction (Fanconi syndrome).. Oculocerebrorenal syndrome is so named because of the prominent involvement ... Organic-aciduria, decreased renal ammonia production, hydrophthalmos, and mental retardation. Am J Dis Child. 1952. 83:164-184 ...
Distal renal tubular acidosis and amelogenesis imperfecta: A rare association. P. Ravi, T. S. Ekambaranath, S. Ellil Arasi, E. ... Contribution of GSTM1, GSTT1, and MTHFR polymorphisms to end-stage renal disease of unknown etiology in Mexicans. ... Successful renal transplantation from a brain-dead deceased donor with head injury, disseminated intravascular coagulation and ... Is bullous skin lesion a risk factor for renal amyloidosis in patients with familial mediterranean fever?. ...
... renal tubular acidosis) are causes of renal calculi or stones. ... renal-kidney-stones&url=renal-kidney-stones-patient-education ... How is a child with renal stones to be monitored?. Children with renal stones should be monitored regularly for symptoms like ... Renal (kidney) Stones. Kumud P Mehta. Consultant Pediatrician & Pediatric Nephrologist, Jaslok Hospital & Research Centre, Bai ... My child has a renal stone, However, he has no complaints. Does he still have to get treated? Cant we just leave him alone?. ...
Cancer, Covid-19, Diabetes, distal renal tubular acidosis, Follicular Lymphoma, hepatitis B, HER2-positive breast cancer, HIV, ... Cancer, Covid-19, Diabetes, distal renal tubular acidosis, Follicular Lymphoma, hepatitis B, HER2-positive breast cancer, HIV, ... for the treatment of distal renal tubular acidosis.. Tukysa (tucatinib) received a positive opinion for the treatment of HER2- ...
... renal tubular acidosis, and inherited tubulopathies, particularly Barrters and Gitelmans syndrome. ... His clinical and research interests are broad and include vascular and hereditary renal disease as well as kidney cancer. He ... Rahbaris research expertise is in the fields of renal cystic diseases and particularly polycystic kidney disease. He has been ... Yu directs a laboratory-based research program that investigates renal tubule physiology and diseases. A current focus is on ...
Renal tubular acidosis. Renal tubular acidosis (RTA) is commonly observed in premature infants. In neonates, the threshold for ... Premature infants require 3-5 mEq/kg/d of sodium, and they may require even more if renal losses are high. ... Sodium deficit causing decreased weight gain and metabolic acidosis in infants with ileostomy. J Pediatr Surg. 1988 Jun. 23(6): ... Increasing the proportion of anions provided as acetate aids in the treatment of metabolic acidosis. Many infants on diuretic ...
Autopsy revealed diffuse pulmonary edema, renal congestion, an eosinophilic substance in renal cortical tubular lumen and ... severe metabolic acidosis, intravascular hemolysis, rhabdomyolysis, methemoglobinemia and oliguria, culminating in renal ... Acute renal failure following paraphenylenediamine (hair dye) poisoning : report of two cases. J. Med 1982; 13: 131-137.. 2. ... Renal collecting tubule and distal tubule epithelium was seen to be necrotic. The blood showed methemoglobinemia (10%). ...
... another renal tubular acidosis or sideroblastic anemia, and another neurological problems - all with the same mt-DNA mutation. ...
Human H+ATPase a4 subunit mutations causing renal tubular acidosis reveal a role for interaction with phosphofructokinase-1. Am ... High rates of tuberculosis in end-stage renal failure: the impact of international migration. Emerg Infect Dis. 2002 Jan; 8(1): ... J Physiol Renal Physiol. 2008 Oct; 295(4):F950-8. Su Y, Blake-Palmer KG, Sorrell S, Javid B, Bowers K, Zhou A, Chang SH, Qamar ...
Targeted deletion of the Ncoa7 gene results in incomplete distal renal tubular acidosis in mice, Brown, D., Breton, S., Oliver ... Renal physiology Y3 - 2007, 2007, 10.1152/ajprenal.00160.2007 * Transcriptomes of major renal collecting duct cell types in ... Renal physiology Y3 -, 2002, 10.1152/ajprenal.00128.2001 * Renal intercalated cells sense and mediate inflammation via the ... Renal physiology Y3 -, 2001, 10.1152/ajprenal.2001.280.3.F426 * The B1-subunit of the H(+) ATPase is required for maximal ...
... renal tubular acidosis, cystinuria, Fanconis), along with common pediatric diagnosis (hematuria and proteinuria). ... Pediatric Renal Transplant program that performs 15-20 new kidney transplants a year and follows approximately 100 post- ... Services include care for children with chronic kidney disease, kidney stones, glomerular disease, tubular disorders ( ...
Renal tubular acidosis (RTA) with calcium stones. *Uric acid lithiasis with or without calcium stones ...
  • The metabolic acidosis that results from RTA may be caused either by insufficient secretion of hydrogen ions (which are acidic) into the latter portions of the nephron (the distal tubule) or by failure to reabsorb sufficient bicarbonate ions (which are alkaline) from the filtrate in the early portion of the nephron (the proximal tubule). (wikipedia.org)
  • Although a metabolic acidosis also occurs in those with chronic kidney disease, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. (wikipedia.org)
  • The metabolic acidosis caused by RTA is a normal anion gap acidosis. (wikipedia.org)
  • Normal anion gap metabolic acidosis/acidemia Hypokalemia, Hypocalcemia, Hyperchloremia Urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate). (wikipedia.org)
  • Reabsorption of bicarbonate is typically 80-90% in the proximal tubule and failure of this process leads to decreased systemic buffer and metabolic acidosis. (wikipedia.org)
  • This chemical imbalance, called metabolic acidosis, can result in a range of signs and symptoms that vary in severity. (medlineplus.gov)
  • A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. (uchicago.edu)
  • Arterial PCO2 in chronic metabolic acidosis. (uchicago.edu)
  • Normal anion gap metabolic acidosis is a common but often misdiagnosed clinical condition associated with diarrhea and renal tubular acidosis (RTA). (karger.com)
  • This review highlights practical aspects concerning normal anion gap metabolic acidosis. (karger.com)
  • Hypocitraturia commonly is observed in patients with nephrolithiasis, metabolic acidosis, and chronic diarrheal syndromes. (medscape.com)
  • There was documented evidence of normal anion gap metabolic acidosis, renal wasting of potassium and hypokalemia in the setting of recent AmBisome. (medcraveonline.com)
  • Toluene inhalation can result in electrolyte and acid-base derangements and should be considered in the differential diagnosis of young patients with unexplained hypokalaemia and normal anion gap metabolic acidosis. (scirp.org)
  • Renal: If untreated, the proximal renal tubular acidosis leads to failure to thrive and metabolic collapse. (medscape.com)
  • A family history of renal stones helps in early diagnosis of certain metabolic disorders which are precursors for stone formation e.g. hypercalciuria which can be detected by 24 hours urine excretion of calcium. (pediatriconcall.com)
  • To alleviate metabolic acidosis, NaHCO 3 infusion was given under arterial blood gas control. (ispub.com)
  • This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses, in particular the renal tubular acidoses (RTAs). (medscape.com)
  • A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. (medscape.com)
  • Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. (medscape.com)
  • Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. (medscape.com)
  • The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). (medscape.com)
  • For this reason, it is also known as hyperchloremic metabolic acidosis. (medscape.com)
  • Go to Metabolic Acidosis, Pediatric Metabolic Acidosis, and Emergent Management of Metabolic Acidosis for complete information on these topics. (medscape.com)
  • Loss of tubular function prevents the kidneys from excreting hydrogen cations (H+) and thereby causes metabolic acidosis. (medscape.com)
  • 10 mEq/L). A urine anion gap of more than 20 mEq/L is seen in metabolic acidosis when the kidneys are unable to excrete ammonia (such as in renal tubular acidosis). (medscape.com)
  • The patient was given intra- ectomy and upper endoscopy are reported venous fluids and potassium to correct his to be associated with Chilaiditi syndrome metabolic acidosis and hypokalaemia. (who.int)
  • The patient continued to have metabolic acidosis and severe hypokalaemia post-surgery for which a nephrology consultation was obtained and the patient was diagnosed as a case of renal tubular acidosis (Table 1). (who.int)
  • In a large Asian series of Distal renal Tubular Acidosis in Sjogren's Syndrome, late diagnosis is a rule in spite of overt hypokalemic periodic paralysis in a vast majority of them dRTA is the most common form of RTA diagnosed in Western countries, and can be classified as either hereditary (primary) or acquired (secondary). (wikipedia.org)
  • Renal histopathology of stone-forming patients with distal renal tubular acidosis. (uchicago.edu)
  • Urine-to-blood carbon dioxide tension gradient and maximal depression of urinary pH to distinguish rate-dependent from classic distal renal tubular acidosis in children. (uchicago.edu)
  • Stone disease in hereditary distal renal tubular acidosis. (uchicago.edu)
  • 2 , 3 Amphotericin B can also cause significant hypokalemia by altering the permeability of distal renal tubular cells, leading to an increase in the passive fluxes of potassium down it electrochemical gradient. (medcraveonline.com)
  • Glue-Sniffing and Distal Renal Tubular Acidosis: Sticking to the Facts," Journal of the American Society of Nephrology, Vol. 1, No. 8, 1991, pp. 1019-1027. (scirp.org)
  • The CHMP also recommended granting a marketing authorisation for Sibnayal (potassium citrate/potassium hydrogen carbonate) for the treatment of distal renal tubular acidosis. (europeanpharmaceuticalreview.com)
  • Because renal excretion is the primary means of eliminating H+ from the body, there is consequently a tendency towards acidemia. (wikipedia.org)
  • Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS. (uchicago.edu)
  • Renal tubular acidosis (RTA) is acidosis and electrolyte disturbances due to impaired renal hydrogen ion excretion (type 1), impaired bicarbonate resorption (type 2), or abnormal aldosterone production or response (type 4). (msdmanuals.com)
  • Emtricitabine and tenofovir are both eliminated by renal excretion. (who.int)
  • Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. (wikipedia.org)
  • Complications of urinary stones are urinary infection and obstruction which may lead to the destruction of renal parenchyma and if the stones are on both sides, they may cause obstruction and destruction of both kidneys. (pediatriconcall.com)
  • Most conditions that affect the kidneys cause a proportionate simultaneous loss of glomerular and tubular function. (medscape.com)
  • Kidney failure , also called renal failure , is when the kidneys slow down or stop properly filtering wastes from the body. (kidshealth.org)
  • An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. (medscape.com)
  • Peripheral neuropathy and lactic acidosis are rare adverse events. (medscape.com)
  • 5.5) and systemic acidosis. (msdmanuals.com)
  • Systemic lupus erythematosus and renal tubular acidosis associated with hyperthyroidism. (nel.edu)
  • Deng D, Sun L, Xia T, Xu M, Wang Y, Zhang Q. Systemic lupus erythematosus and renal tubular acidosis associated with hyperthyroidism. (nel.edu)
  • In patients with significant hyperkalemia one should evaluate for RTA type 4, especially in diabetic patients, with a relatively conserved renal function. (karger.com)
  • Ibuprofen is contraindicated in patients with severe heart failure (NYHA Class IV), hepatic failure and renal failure (see section 4.4). (medicines.org.uk)
  • Life expectancy: Patients with appropriate therapy may live to be 30-40 years of age, generally dying from renal failure, respiratory distress, status epilepticus, or infection. (medscape.com)
  • Pediatric Renal Transplant program that performs 15-20 new kidney transplants a year and follows approximately 100 post-transplant patients. (umich.edu)
  • This test is most commonly performed in patients who present with altered mental status, unknown exposures, acute renal failure, and acute illnesses. (medscape.com)
  • Patients with renal stones who require endoscopic laser treatment in the outpatient operating room. (who.int)
  • Patients' stone size in a single renal unit of greater than or equal to 5 millimeters (mm) and less than or equal to 20 mm. (who.int)
  • Yet risks of renal failure and renal replacement therapy were similar in patients treated with nucleoside analogues versus nucleotide analogues in real-life setting. (medscape.com)
  • Thus, exposure to both compounds increases in patients with renal dysfunction. (who.int)
  • Therefore, in patients with renal impairment [HA552 trade name] should only be used if the potential benefits of treatment are considered to outweigh the potential risks. (who.int)
  • Patients with renal impairment may require close monitoring of renal function (see section 4.4). (who.int)
  • Limited data from clinical studies support once daily dosing of [HA552 trade name] in patients with mild renal impairment (see section 4.4). (who.int)
  • It also causes rhabdomyolysis and acute renal failure, culminating in death if not treated aggressively 2 . (ispub.com)
  • In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine. (wikipedia.org)
  • Each nephron consists of two parts: a renal corpuscle (also known as a glomerulus) that filters the blood, and a renal tubule that reabsorbs substances that are needed and eliminates unneeded substances in urine. (medlineplus.gov)
  • Services include care for children with chronic kidney disease, kidney stones, glomerular disease, tubular disorders (renal tubular acidosis, cystinuria, Fanconi's), along with common pediatric diagnosis (hematuria and proteinuria). (umich.edu)
  • The term hyperchloremic acidosis (ie, RTA) refers to a diverse group of tubular disorders, uncoupled from glomerular damage, characterized by impairment of urinary acidification without urea and anion retention. (medscape.com)
  • We report the first case of Chilaiditi laparotomy, the patient was found to have syndrome caused by adynamic ileus result- hugely distended bowel loops extending ing from hypokalaemia induced by renal from the ligament of Treitz down to the tubular acidosis. (who.int)
  • In this case, the cause of ileus was severe hypokalaemia resulting from type-1 renal tubular acidosis. (who.int)
  • If the anion gap is found to be high, other tests such as urine ketones, serum ketones (beta-hydroxybutyrate), serum lactic acid, urine drug screen, serum drug screen, salicylate level, and creatinine kinase level should also be performed to diagnose the etiology of the anion gap acidosis. (medscape.com)
  • For HIV-therapy administration of [HA552 trade name] every 48 hours is recommended, based on modelling of single-dose pharmacokinetic data for emtricitabine and tenofovir disoproxil in non-HIV infected subjects with varying degrees of renal impairment (see section 4.4). (who.int)
  • A normal AG acidosis is characterized by a lowered bicarbonate concentration, which is counterbalanced by an equivalent increase in plasma chloride concentration. (medscape.com)
  • Proximal RTA (pRTA) is caused by a failure of the proximal tubular cells to reabsorb filtered bicarbonate from the urine, leading to urinary bicarbonate wasting and subsequent acidemia. (wikipedia.org)
  • There is a risk of renal impairment in dehydrated children and adolescents. (medicines.org.uk)
  • It is characterized by congenital cataracts, infantile glaucoma, neonatal or infantile hypotonia, intellectual impairment, and renal tubular dysfunction (Fanconi syndrome). (medscape.com)
  • The long-term safety of tenofovir and emtricitabine in mild renal impairment (creatinine clearance 50-80 mL/minute) has not been fully assessed. (who.int)
  • The primary indication for kidney transplantation is End-stage renal failure. (msdmanuals.com)
  • An increased value of the AG suggests a possible organic acidosis due to endogenous acids or exposure to exogenous acids [ 1 ]. (karger.com)
  • Obstructive Uropathy Obstructive uropathy is structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction (obstructive nephropathy). (msdmanuals.com)
  • A positive urine anion gap is seen in conditions of type 1 and type 2 renal tubular acidosis versus almost every other cause of normal anion gap acidosis (diarrhea). (medscape.com)
  • Most children and adults with renal tubular acidosis with deafness have short stature, and many develop kidney stones . (medlineplus.gov)
  • In addition, a renal tubular defect that reduces reabsorption may alter phosphate metabolism. (medscape.com)
  • 4 Liposomal formulation of Amphotericin B has been proposed to be associated with less renal toxicity. (medcraveonline.com)
  • Bone toxicity is closely related to nucleoside analogue effect on renal proximal tubular and phosphaturia. (medscape.com)
  • Conventional form of Amphotericin B has been associated with renal tubular acidosis, decreased renal function and hypokalemia. (medcraveonline.com)
  • AmBisome has been known to cause both significant hypokalemia and decreased renal function that was presumed to be the cause in our patient. (medcraveonline.com)
  • Certain areas are known for increased prevalence for renal calcium or urolithiasis because of the hot climate, excess of calcium/manganese/aluminum, and many other minerals in soil/water which increases the solute load. (pediatriconcall.com)
  • Renal collecting duct physiology and pathophysiology 1 . (bvsalud.org)
  • By the second to third decade, gradual loss of creatinine clearance occurs, with progressive renal failure . (medscape.com)
  • In the long run, chronic renal failure (CRF) can occur. (pediatriconcall.com)
  • Here we report a case of suicidal ingestion of this hair dye, resulting in rapidly developing massive edema of neck and face, respiratory distress, seizures and death due to renal failure. (ispub.com)
  • In renal tubular acidosis with deafness, enlarged vestibular aqueduct typically occurs in individuals whose hearing loss begins in childhood. (medlineplus.gov)
  • Commonly these symptoms occur due to urinary tract infection and in absence of fever, renal stones should be ruled out. (pediatriconcall.com)
  • The newly approved tenofovir alafenamide (TAF) has improved renal and bone safety profiles compared to TDF. (medscape.com)
  • Chronic Kidney Disease Chronic kidney disease (CKD) is long-standing, progressive deterioration of renal function. (msdmanuals.com)
  • Mutations in the ATP6V1B1 or ATP6V0A4 gene impair the function of the V-ATPase complex and reduce the body's capability to control the pH of the blood and the fluid in the inner ear, resulting in the signs and symptoms of renal tubular acidosis with deafness. (medlineplus.gov)
  • Female carriers manifest characteristic lens opacities, but they typically have normal renal and neurologic function. (medscape.com)
  • The impression was renal tubular acidosis type I secondary to recent AmBisome use. (medcraveonline.com)
  • The word acidosis refers to the tendency for RTA to cause an excess of acid, which lowers the blood's pH. (wikipedia.org)

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